Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Nurs 216 > perfusion > Flashcards

perfusion Flashcards

1
Q

what is cardiovascular disease linked to

A

closely linked to diet

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

hormonal and NS factors affecting BP

A

adrenal gland, kidney, hypothalamus, baroreceptors, vasomotor centre in medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

baroreceptors

A

mechanoreceptors on the heart which are stimulated by changes in the stretch of the carotid sinus wall. stimulates vasomotor centre in medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

vasomotor centre in medulla (low bp)

A

stimulated by baroreceptors and release norepinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

norepinephrine

A

vasoconstrictor. released from vasomotor centre in medulla and adrenal gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

factors that influence BP (3)

A

blood volume, peripheral resistance, and cardiac output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Blood Volume determined by

maintained by

A

amount of water and sodium ingested

maintained by kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

how does blood volume influence BP

A 
fluid loss (dehydration) decreases blood volume = low BP
fluid retention (by aldosterone or ADH) increases blood volume=high BP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how does peripheral resistance influence BP (3)

A
  • Sympathetic nervous system innervation
  • renin/angiotensin ii
  • increased blood viscosity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

sympathetic NS innervation

A

causes vasoconstriction (=increase BP) or vasodilation (=decrease BP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

renin/angiotensin II

action of angiotensin II

A
  • renin (from kidneys) + angiotensinogen (liver) = angiotensin I + angiotensin converting enzyme (ACE) = angiotensin II
  • angiotensin II binds to receptors on blood vessels, heart, adrenal cortex causing vasoconstriction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

increase in blood viscosity

A

increase in hematocrit = increase viscosity

increase in blood viscosity causes resistance in blood vessels = high BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

vasoconstriction cascade

what starts it

A

systemic vasoconstriction, aldosterone synthesis, H20&Na retention
caused when angiotensin II binds to receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what happens when angiotension II pathway is blocked

A

if pathway is blocked, angiotensinogen isn’t converted and vasoconstriction cascade is not activated = decrease BP & blood volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

how does cardiac output influence BP (2)

A
  • stroke volume

- heart rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Stroke volume

influenced by

A
  • amount of blood thats pumped out the left side of the heart to the body
  • preload, contractility, afterload
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

increase SV

A

more blood pumped out of the body = high BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

decrease SV

A

less blood pumped out of body=low BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what influences heart rate

A

sympathetic NS, parasympathetic NS & epinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

actions of heart when BP is too high (3)

A
  • vasodilation
  • low SV
  • low HR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

actions of kidneys due to high BP (2)

A
  • high urine output

- low blood volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

hypertension

A

elevation of systolic &/or diastolic BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

BP to worry about (2)

A

<160 mmhg too high

sudden change >20mmh

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

causes of sudden change in BP (6)

A

pain, infection, compensation, hypervolemia, drug induced, malignant hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

circadian BP variations

A

reason why BP is graphed. assess trends to determine chronic changes in BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

causes of hypertension (3)

A
  • essential
  • secondary
  • sudden onset
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

(causes) essential hypertension (4)

A

(idiopathic) age, race, family history, lifestyle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

(causes) secondary hypertension

A

due to organ not working properly; renal disease, adrenal disease, congenital defects; other end organ disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

(causes) sudden onset

A

sudden onset of hypertension due to meds, recreational drugs, or trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

gestational hypertension

A

preeclampsia- at 20 weeks pregnant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

gestational hypertension causes

A

multifocal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

inflammatory theory of cause of hypertension

A

inflammatory cytokine released causes endothelial changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

risk of endothelial changes that cause gestational hypertension (4)

A

clotting (to fix damage), risk of DIC, organ damage, and decreased placental flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

gestational hypertension tx

A

sodium restriction & antihypertensive medication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

causes of hypertension in elderly (3)

A

decreased elasticity of vessels, decreased renal blood flow, decreased baroreceptors sensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

tx of hypertension in elderly (3)

A

start low and go slow, “titrate to effect”, & monitor for orthostatic hypotension (risk of falls)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

orthostatic hypotension

A

drop of SBP >20 mmHg or DBP >10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

orthostatic hypotension causes

A

caused by venous pooling in lower extremities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

nature of orthostatic hypotension

A

transient since baroreceptors have low sensitivity, compensated when they intervene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

orthostatic hypotension S&S (2)

A

faintness, dizziness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

at risk for orthostatic hypotension (3)

A

-elderly, dehydrated patients, patients on antihypertensive meds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

orthostatic hypotension tx (2)

A

have to treat the underlying cause, adrenergic agonists if in the ER

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

lifestyle changes for hypertension (3)

A

decrease cholesterol and alcohol intake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

organs affected by hypertension (5)

A

brain, eyes, kidney, placenta, liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

expected BP findings & MAP

A

BP: 120/80 mmHg MAP: 70-100 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

blood pressure

A

perfusion of tissue and organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

MAP

A

mean arterial pressure, used to measure adequate amount of blood getting to vital tissues and organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

MAP formula

A

SP+2(DP)/3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Emergency tx of hypertension

drug class

A

treatment stimulates endothelial cell-produced endogenous NITRIC OXIDE
direct acting vasodilator

50
Q

how is nitric oxide produced

A

converted in endothelial cell by arginine into NO then enters the smooth muscle cell activating cyclic GMP pathway causing

51
Q

direct acting vasodilator function

A

stimulates nitric oxide release in endothelium

52
Q

direct acting vasodilator uses

A

only used in ICU of ER settings

53
Q

direct acting vasodilator routes

A

IV- 2 min 1/2 life

inhalation- broncho specific

54
Q

direct acting vasodilator examples (2)

A

nipride, hydralazine

55
Q

direct acting vasodilator s/e

A

reflex tachycardia (hypotension), syncope, headache

56
Q

nipride & function

routes

A

nitroprusside; stimulates nitric oxide release in endothelium
-IV continuous infusion in crisis, endotracheal tube for pulmonary vasodilation

57
Q

hydralazine function & routes

A

stimulates nitric oxide release in endothelium\

PO/IV

58
Q

hypertension standard treatment meds classes (4)

A

diuretics, renin-angiotensin drugs, calcium channel blockers, adrenergic agents

59
Q

hypertension standard treatment meds (combo drugs)

A

direct acting vasodilators (ER use), synergy effect

60
Q

1st line hypertension tx

A

diuretics

61
Q

diuretics functions (5)

A
  • decreases blood volume, BP, H20 & electrolytes

- increases urine output

62
Q

types of diuretics (4)

A

loop diuretics, thiazides, potassium sparing, osmotic

63
Q

diuretics s/e

A

dehydration, hypoatremia, hypokalemia, hyperkalemia, nocturia

64
Q

loop diuretics target

A

loop of henle

65
Q

loop diuretics function

A

blocks Na+, K+, Cl- reabsorption into blood so Na, K, Cl & H20 stay inside tubule and get excreted as urine

66
Q

loop diuretics s/e

A

hypokalemia (K excreted with urine), ototoxicity (can be reversible with drug interactions (high PPB))

67
Q

most potent route for loop diuretics

A

IV, PO

68
Q

loop diuretics example

A

furosemide

69
Q

furosemide

A

(lasix) first line of therapy for hypertension, blocks sodium potassium chloride cotransporter stopping Na, K, Cl & H20 from exiting tubule so they’re excreted with urine

70
Q

thiazides target

A

distal convoluted tubule

71
Q

thiazides function

A

inhibits reabsorption of Na and Cl out of tubule = increase Na, Cl, K & H20 in urine

72
Q

thiazides s/e

A

hypokalemia, hyponatremia

73
Q

thiazide examples

A

hydrochlorothyazide, chlorothyazide

74
Q

metabolism of thiazides

A

unchanged

75
Q

potassium sparing function

A

(aldosterone antagonist) blocks renal aldosterone receptors = Na exits and K stays

76
Q

potassium sparing target

A

distal tubule

77
Q

potassium sparing s/e

A

hyperkalemia

78
Q

metabolism of potassium sparing

A

active metabolites, long half life (1-2 days)

79
Q

potassium sparing example

A

spironolactone (aldactone)

80
Q

diuretic combo

A

aldactazide (thiazide + potassium sparing)

81
Q

aldactazide uses

A

maintenance therapy for hypertension, balances out K

PO

82
Q

osmotics target

A

proximal tubule & loop of henle

83
Q

osmotics function

A

drug contains high solute so to prevents reabsorption of water into blood = low blood volume = low bp

84
Q

osmotic tx

A

cerebral edema, intraocular hypotension

85
Q

angiotensin ii drugs (2)

A

angiotensin ii receptor blockers (ARB), angiotensin-converting enzyme inhibitors (ACE inhibitors)

86
Q

ARB site of action

A

angiotensin ii receptors

87
Q

what does blocking of angiotensin ii receptors cause

A

prevents vasoconstriction cascade= lowers BP

88
Q

ARB examples

A

losartan

89
Q

ARB s/e

A

hypotension

90
Q

ACE inhibitor fx

A

inhibit ACE from producing angiotensin ii= reduce vasoconstriction

91
Q

1st line drugs in heart failure

A

ACE inhibitors

92
Q

ACE inhibitor examples

A

enalapril, captopril, monopril, ramipril

93
Q

ACE inhibitor s/e

A

severe hypotension

94
Q

hyazaar

A

losartan + hydrochlorothiazide

95
Q

osmotics ex

A

mannitol (IV) , isosorbide (PO)

96
Q

calcium channel blocker fx

A

prevents calcium influx causing muscle relaxation

97
Q

types of calcium channel blockers

A

vascular selective, cardio-selective

98
Q

vascular selective ccb fx

A

vasodilation of blood vessels around the body

99
Q

vascular selective ccb ex

A

nifedipine, amlodipine

100
Q

cardio selective ccb fx

A

cause relaxation of myocardial cells which decreases HR, CO and BP

101
Q

cardio selective ccb ex

A

verapamil, diltiazem

102
Q

adrenergic antagonists fx

A

block sympathetic ns function; decrease HR, conduction rate and contractility

103
Q

adrenergic antagonists targets

A

alpha (1 & 2), beta (1 & 2) receptors

104
Q

alpha receptors fx

A

cause vasoconstriction of blood vessels

105
Q

alpha 1 receptors

A

bind with norepinephrine to cause vasoconstriction of blood vessels

106
Q

alpha 2 receptors

A

in arteries and veins stimulation causes vasoconstriction

in CNS stimulation releases norepinephrine which cause vasoconstriction

107
Q

beta 1 receptors

A

located in pacemakers cells and myocardial cells in heart, stimulation causes increased heart rate, increased contractility, increased conduction rate, and vasodilation

108
Q

beta 2 receptors

A

located in bronchioles cause bronchodilation

109
Q

beta blockers fx

A

decrease conduction rate & contractility= low HR = low bp

110
Q

selective beta blockers ex

A

atenolol, metoprolol

111
Q

nonselective beta blockers

A

propanolol

112
Q

beta blocker s/e

A

bradycardia, lethargy, hypotension

113
Q

lopresser HCT

A

hydrochlorothiazide + metaprolol

114
Q

centrally acting alpha 2 agonist fx

A

stimulate cns alpha 2 receptors in vasomotor center to activate negative feedback lopp and decrease norepinephrine release

115
Q

centrally acting alpha 2 agonist ex

A

clonidine, methyldopa

116
Q

methyldopa

A

prodrug, metabolizes into norepinephrine and activates negative feedback loop

117
Q

centrally acting alpha 2 agonist s/e

A

hypotension and headaches

118
Q

centrally acting alpha 2 agonist tx’s

A

resistant hypertension

119
Q

atrial fibrillation medications

A

calcium channel blockers (verapamil, diltiazem) & beta blockers (propanolol, metoprolol)

120
Q

Calcium channel blockers s/e

A

dizziness, hypotension, reflex tachycardia,, peripherial edema, dysrhythmias, exacerbation of heart failure

Nurs 216 (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions